Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models

Liguori, Gabriel Romero; Kanas, Alexandre Fligelman; Moreira, Luíz Felipe Pinho

doi:10.5935/1678-9741.20140017

Cited by 13 publications

(13 citation statements)

References 71 publications

(72 reference statements)

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“…effect, which has a short half-life (1.5 to 2 hours), not only on the postoperative inflammatory activity of serum hsCRP, TNF-alpha and VEGF, but also on TNF-alpha and VEGF in the carotid plaque. Previous publications have already demonstrated that glucocorticoids can interfere in the systemic inflammatory response, reducing concentrations of serum biomarkers and attenuating activation of the complement system and leukocyte and neutrophil adhesion, 13,14 but this effect has not been demonstrated with respect to hsCRP, TNF-alpha or VEGF, and the action of glucocorticoids on the behavior of biomarkers present in patients treated with EAC has not been assessed. After administering 30 mg/kg of intravenous methylprednisolone before surgery and before unclamping the thoracic aorta in 16 patients treated with revascularization of the myocardium, Kawamura et al 15 observed reductions in plasma concentrations of interleukins IL-6 and IL-8 at 1 hour, 2 hours and 3 hours after the aorta was unclamped.…”

Section: Discussionmentioning

confidence: 99%

Hidrocortisona reduz as concentrações séricas dos biomarcadores inflamatórios séricos em pacientes submetidos a endarterectomia de carótida

et al. 2015

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Background: Hydrocortisone may reduce serum and tissue concentrations of inflammatory biomarkers. Objective: To analyze the inflammatory activity of serum and tissue high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor (TNF)-α and vascular endothelial growth factor (VEGF) after intraoperative administration of hydrocortisone, after carotid endarterectomy (CEA). Method: Twenty-two patients were allocated to a Control Group (5 asymptomatic and 6 symptomatic patients) and were not administered hydrocortisone or to Group 1 (4 asymptomatic and 7 symptomatic patients) and were administered 500 mg intravenous hydrocortisone. Serum levels of hsCRP, TNF-α and VEGF were tested for the preoperative period and at 1 hour, 6 hours and 24 hours after CEA. Levels of TNF-α and VEGF were also measured in carotid plaques. Results: Group 1 exhibited lower concentrations of serum TNF-α at 1 hour (p=0.031), 6 hours (p=0.015) and 24 hours (p=0.017) after CEA and lower concentrations of serum VEGF at 1 hour (p=0.006) and 6 hours (p=0.005) after CEA, relative to controls. Symptomatic patients in group 1 exhibited lower concentrations than controls for serum TNF-α at 1 hour and 6 hours after CEA and lower concentrations than controls for serum VEGF at 1 hour after CEA. There were no statistical differences in tissue concentrations of TNF-α or VEGF between the control group and group 1. Conclusion: Hydrocortisone reduces postoperative concentrations of serum TNF-α and VEGF, especially in symptomatic patients; but does not reduce tissue levels of these biomarkers.

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Section: Discussionmentioning

confidence: 99%

Hidrocortisona reduz as concentrações séricas dos biomarcadores inflamatórios séricos em pacientes submetidos a endarterectomia de carótida

et al. 2015

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“…Furthermore, the persistence of any degree of inflammation may be considered potentially harmful to the cardiovascular patient submitted to surgery [ 14 ] . Rubens & Messana [ 15 ] and Liguori et al [ 16 ] have concluded that the systemic inflammatory response is variable and is influenced by comorbidities exhibited by patients, non-pharmacological intervention during surgery, type of anesthesia, perioperative hemodynamic conditions, surgical aspects (surgical incision, duration, time of arterial crossclamping and need for blood transfusion) and postoperative evolution. In this study, we standardized general anesthesia and classical CEA with longitudinal arteriotomy, in order to keep our patients under the same perioperative conditions.…”

Section: Discussionmentioning

confidence: 99%

Hydrocortisone Supresses Inflammatory Activity of Metalloproteinase-8 in Carotid Plaque

Gabriel

Antonângelo

Capelozzi

et al. 2015

Revista Brasileira De Cirurgia Cardiovascular

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ObjectiveMatrix metalloproteinases are inflammatory biomarkers involved in carotid plaque instability. Our objective was to analyze the inflammatory activity of plasma and carotid plaque MMP-8 and MMP-9 after intravenous administration of hydrocortisone.MethodsThe study included 22 patients with stenosis ≥ 70% in the carotid artery (11 symptomatic and 11 asymptomatic) who underwent carotid endarterectomy. The patients were divided into two groups: Control Group - hydrocortisone was not administered, and Group 1 - 500 mg intravenous hydrocortisone was administered during anesthetic induction. Plasma levels of MMP-8 and MMP-9 were measured preoperatively (24 hours before carotid endarterectomy) and at 1 hour, 6 hours and 24 hours after carotid endarterectomy. In carotid plaque, tissue levels of MMP-8 and MMP-9 were measured.ResultsGroup 1 showed increased serum levels of MMP- 8 (994.28 pg/ml and 408.54 pg/ml, respectively; P=0.045) and MMP-9 (106,656.34 and 42,807.69 respectively; P=0.014) at 1 hour after carotid endarterectomy compared to the control group. Symptomatic patients in Group 1 exhibited lower tissue concentration of MMP-8 in comparison to the control group (143.89 pg/ml and 1317.36 respectively; P=0.003). There was a correlation between preoperative MMP-9 levels and tissue concentrations of MMP-8 (P=0.042) and MMP-9 (P=0.019) between symptomatic patients in the control group.ConclusionHydrocortisone reduces the concentration of MMP- 8 in carotid plaque, especially in symptomatic patients. There was an association between systemic and tissue inflammation.

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“…Phosphodiesterase-5 (PDE5) has the most desirable characteristics to be inhibited if secondary vascular and coagulation profile are to be preserved for a longer period. Therefore, if systemic actions are intended, as the needed in MOFS, it must be used a PDE5 inhibitor, that will maintain the NO-induced cGMP activation functioning for a long period, in the entire organic system [ 22 , 26 ] .…”

Section: Introductionmentioning

confidence: 99%

Tadalafil: Protective Action against the Development of Multiple Organ Failure Syndrome

Oliveira¹,

Oliveira²,

Botelho³

et al. 2017

Braz J Cardiovasc Surg

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IntroductionMultiple organ failure syndrome (MOFS) is a pathology associated to unspecified and severe trauma, characterized by elevated morbidity and mortality. The complex inflammatory MOFS-related reactions generate important ischemia-reperfusion responses in the induction of this syndrome. Nitric oxide elevation, through the activation of cyclic guanosine monophosphate (cGMP), has the potential of counteracting the typical systemic vasoconstriction, and platelet-induced hypercoagulation. Tadalafil would possibly act protectively by reducing cGMP degradation with consequent diffuse vasodilatation, besides reduction of platelet-induced hypercoagulation, thus, preventing multiple organ failure syndrome development.MethodsThe experimental protocol was previously approved by an institution animal research committee. Experimental MOFS was induced through the stereotaxic micro-neurosurgical bilateral anterior hypothalamic lesions model. Groups of 10 Wistar rats were divided into:a) Non-operated control;b) Operated control group;c) 2 hours after tadalafil-treated operated group;d) 4 hours after tadalafil-treated operated group;e) 8 hours after post-treated operated group. The animals were sacrificed 24 hours after the neurosurgical procedure and submitted to histopathologic examination of five organs: brain, lungs, stomach, kidneys, and liver.ResultsThe electrolytic hypothalamic lesions resulted in a full picture of MOFS with disseminated multiple-organs lesions, provoked primarily by diffusely spread micro-thrombi. The treatment with tadalafil 2 hours after the micro-neurosurgical lesions reduced the experimental MOFS lesions development, in a highly significant level (P<0.01) of 58.75%. The treatment with tadalafil, 4 hours after the micro-neurosurgically-induced MOFS lesions, also reduced in 49.71%, in a highly significant level (P<0.01). Finally, the treatment with tadalafil 8 hours after the neurosurgical procedure resulted in a statistically significant reduction of 30.50% (P<0.05) of the experimentally-induced MOFS gravity scores.ConclusionThe phosphodiesterase 5 inhibitor, tadalafil, in the doses and timing utilized, showed to protect against the experimentally-induced MOFS.

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Managing the inflammatory response after cardiopulmonary bypass: review of the studies in animal models

Cited by 13 publications

References 71 publications

Hidrocortisona reduz as concentrações séricas dos biomarcadores inflamatórios séricos em pacientes submetidos a endarterectomia de carótida

Hidrocortisona reduz as concentrações séricas dos biomarcadores inflamatórios séricos em pacientes submetidos a endarterectomia de carótida

Hydrocortisone Supresses Inflammatory Activity of Metalloproteinase-8 in Carotid Plaque

Tadalafil: Protective Action against the Development of Multiple Organ Failure Syndrome

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